)| PMID |
12124437 ( ) |
|---|---|
| Title | Temporal patterns of cytokine and apoptosis-related gene expression in spinal cords of the G93A-SOD1 mouse model of amyotrophic lateral sclerosis. |
| Abstract | Familial amyotrophic lateral sclerosis (FALS) is often caused by gain-of-function mutations in Cu,Zn-superoxide dismutase (SOD1). Multiprobe ribonuclease protection assays (RPAs) were used to investigate expression of 36 different cytokines and apoptosis-related genes in spinal cords of mice that ubiquitously express human SOD1 bearing a glycine (r) alanine substitution at residue 93 (G93A-SOD1). Mice were studied at late presymptomatic stage (80 days), and at 120 days when the animals experience severe hindlimb paralysis and accumulation of oxidatively modified proteins. Spinal cord tissue from G93A-SOD1 mice expressed a selective subset of macrophage-typical cytokines (monokines) including interleukin (IL)1alpha, IL1beta and IL1RA at 80 days increasing by 120 days. Contrastingly, T-cell derived cytokines (lymphokines) including IL2, IL3 and IL4 were detected at low levels in non-transgenic mice but these were not elevated in G93A-SOD1 mice even at 120 days. Apoptosis-related genes were generally unaffected at 80 days but multiple caspases and death receptor components were up-regulated at 120 days; the only exceptions being FADD and the tumor necrosis factor (TNF)alpha receptor p55 which was up-regulated at 80 days and increased further at 120 days. These data indicate that in the G93A-SOD1 mouse: (i) cytokine expression changes precede bulk protein oxidation and apoptosis gene expression; (ii) lymphocyte contributions to cytokine expression in FALS are likely minor; and (iii) TNFalpha and its receptors may link inflammation to apoptosis in ALS. Foundation, Oklahoma City, Oklahoma 73104, USA. Kenneth-Hensley@omrf.ouhsc.edu |
NOTE: Color highlight is limited to the abstract and SciMiner text-mining mode. If you see much more identified targets below from "Targets by SciMiner Summary" and "Targets by SciMiner Full list", they may have been identified from the full text.
Targets by SciMiner Summary
| HUGO ID | Symbol | Target Name | #Occur | ActualStr |
|---|---|---|---|---|
| 11892 | TNF | tumor necrosis factor (TNF superfamily, member 2) | 6 | tumor necrosis factor | TNFalpha | tnf alpha | TNF | |
| 11179 | SOD1 | superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult)) | 3 | SOD1 | superoxide dismutase | |
| 6014 | IL4 | interleukin 4 | 2 | IL4 | |
| 5993 | IL1R1 | interleukin 1 receptor, type I | 1 | IL1RA | |
| 5992 | IL1B | interleukin 1, beta | 1 | IL1beta | |
| 3573 | FADD | Fas (TNFRSF6)-associated via death domain | 1 | FADD | |
| 11916 | TNFRSF1A | tumor necrosis factor receptor superfamily, member 1A | 1 | p55 | |
| 6001 | IL2 | interleukin 2 | 1 | IL2 | |
| 6011 | IL3 | interleukin 3 (colony-stimulating factor, multiple) | 1 | IL3 | |
Targets by SciMiner Full list
| HUGO ID | Symbol | Name | ActualStr | Score | FlankingText |
|---|---|---|---|---|---|
| 11179 | SOD1 | superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult)) | SOD1 | 1.4 | often caused by gain-of-function mutations in Cu Zn-superoxide dismutase (SOD1) SOD1 |
| 11179 | SOD1 | superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult)) | SOD1 | 1.4 | genes in spinal cords of mice that ubiquitously express human SOD1 bearing a glycine (r) r alanine substitution at residue 93 |
| 5992 | IL1B | interleukin 1, beta | IL1beta | 0.3 | of macrophage-typical cytokines (monokines) monokines including interleukin (IL)1alpha, IL 1alpha IL1beta and IL1RA at 80 days increasing by 120 days |
| 5993 | IL1R1 | interleukin 1 receptor, type I | IL1RA | 1.3 | cytokines (monokines) monokines including interleukin (IL)1alpha, IL 1alpha IL1beta and IL1RA at 80 days increasing by 120 days |
| 6001 | IL2 | interleukin 2 | IL2 | 0.3 | Contrastingly T-cell derived cytokines (lymphokines) lymphokines including IL2 IL3 and IL4 were detected at low levels in non-transgenic |
| 6011 | IL3 | interleukin 3 (colony-stimulating factor, multiple) | IL3 | 0.3 | Contrastingly T-cell derived cytokines (lymphokines) lymphokines including IL2 IL3 and IL4 were detected at low levels in non-transgenic mice |
| 6014 | IL4 | interleukin 4 | IL4 | 0.3 | Contrastingly T-cell derived cytokines (lymphokines) lymphokines including IL2 IL3 and IL4 were detected at low levels in non-transgenic mice |
| 6014 | IL4 | interleukin 4 | IL4 | 0.3 | Contrastingly T-cell derived cytokines (lymphokines) lymphokines including IL2 IL3 and IL4 were detected at low levels in non-transgenic mice but these |
| 3573 | FADD | Fas (TNFRSF6)-associated via death domain | FADD | 1.6 | components were up-regulated at 120 days the only exceptions being FADD and the tumor necrosis factor (TNF)alpha TNF alpha receptor p55 |
| 11892 | TNF | tumor necrosis factor (TNF superfamily, member 2) | TNF | 1.2 | only exceptions being FADD and the tumor necrosis factor (TNF)alpha TNF alpha receptor p55 which was up-regulated at 80 days and |
| 11916 | TNFRSF1A | tumor necrosis factor receptor superfamily, member 1A | p55 | 1.2 | FADD and the tumor necrosis factor (TNF)alpha TNF alpha receptor p55 which was up-regulated at 80 days and increased further at |
| 11892 | TNF | tumor necrosis factor (TNF superfamily, member 2) | TNFalpha | 1.2 | cytokine expression in FALS are likely minor and (iii) iii TNFalpha and its receptors may link inflammation to apoptosis in ALS |
| 11179 | SOD1 | superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult)) | superoxide dismutase | 1.0 | familial amyotrophic lateral sclerosis fals is often caused by gain of function mutations in cu zn superoxide dismutase sod1 . |
| 11892 | TNF | tumor necrosis factor (TNF superfamily, member 2) | tnf alpha | 1.0 | osis related genes were generally unaffected at 80 days but multiple caspases and death receptor components were up regulated at 120 days; the only exceptions being fadd and the tumor necrosis factor tnf alpha receptor p55 which was up regulated at 80 days and increased further at 120 days. |
| 11892 | TNF | tumor necrosis factor (TNF superfamily, member 2) | tumor necrosis factor | 1.0 | apoptosis related genes were generally unaffected at 80 days but multiple caspases and death receptor components were up regulated at 120 days; the only exceptions being fadd and the tumor necrosis factor tnf alpha receptor p55 which was up regulated at 80 days and increased further at 120 days. |
| 11892 | TNF | tumor necrosis factor (TNF superfamily, member 2) | tumor necrosis factor | 1.0 | tor proteins signal transducing|antigens cd|carrier proteins|cytokines|fadd protein human|fadd protein mouse|fas associated death domain protein|lymphokines|monokines|proteins|rna messenger|receptors tumor necrosis factor|receptors tumor necrosis factor type i|sod1 g93a protein|superoxide dismutase|caspases| |
| 11892 | TNF | tumor necrosis factor (TNF superfamily, member 2) | tumor necrosis factor | 1.0 | |receptors tumor necrosis factor type i|sod1 g93a protein|superoxide dismutase|caspases| |